I. Field of the Invention
The present invention relates generally to implantable and external cardiac rhythm management devices, and more particularly relates to a method and apparatus for attenuating polarization voltages or "afterpotentials" which develop at the lead's electrodes following the delivery of a stimulus to the heart tissue from a pulse generator of the cardiac rhythm management device. The reduction in the effects of afterpotentials enhances the ability to determine whether the stimulus evokes a response in the heart or results in heart capture or contraction while utilizing electrodes for both pacing and sensing, and thereby facilitates improved tracking of the capture threshold for minimizing power consumption while assuring therapeutic efficacy.
II. Discussion of the Prior Art
Cardiac rhythm management devices have enjoyed widespread use and popularity through time as a means for supplanting some or all of an abnormal heart's natural pacing functions. Among the various heart abnormalities remedied by pacemakers include total or partial heart block, arrhythmias, myocardial infarctions, congestive heart failure, congenital heart disorders, and various other rhythm disturbances within the heart. The fundamental components of a cardiac pacemaker include an electronic pulse generator for delivering stimulus pulses to the heart and an electrode lead arrangement (unipolar or bipolar) for sensing evoked responses and intrinsic events from the heart.
Depending upon the heart abnormality, cardiac pacemakers may be designed to engage in ventricular pacing, atrial pacing, or dual chamber pacing in both the atrium and ventricle. Regardless of the type of cardiac pacemaker employed to restore the heart's natural rhythm, all operate to stimulate heart tissue cells adjacent to the electrode of the pacing lead which is employed in the heart and electrically coupled to the pacemaker. When the stimulus evokes a response in the heart, this response is typically referred to as "capture" and is a function of the positive and negative charges found in each myocardial cell within the heart.
More specifically, when a stimulus that evokes a response is applied to the cell membrane, the selective permeability of the cell membrane is disturbed such that it can no longer block the inflow of sodium ions from outside the cell membrane. The inflow of sodium ions at the stimulation site causes the adjacent portions of the cell membrane to lose its selective permeability, thereby causing a chain reaction across the cell membrane until the cell interior is flooded with sodium ions. This process, referred to as depolarization, causes the myocardial cell to have a net positive charge due to the inflow of sodium ions. The electrical depolarization of the cell interior causes a mechanical contraction or shortening of the myofibril of the cell membrane. The syncytial structure of the myocardium will cause the depolarization originating in any one cell to radiate through the entire mass of the heart muscle so that all cells are stimulated for effective pumping. Following heart contraction or systole, the selective permeability of the cell membrane returns and sodium is pumped out until the cell is repolarized with a negative charge within the cell membrane. This causes the cell membrane to relax and return to the fully extended state, referred to as diastole.
Once in diastole, the success of a cardiac pacemaker in depolarizing or "capturing" the heart hinges on whether the energy of the pacing stimulus as delivered to the myocardium exceeds a threshold value. This threshold value, referred to as the capture threshold, represents the amount of electrical energy required to alter the permeability of the myocardial cells to thereby initiate cell depolarization. If the energy of the pacing stimulus does not exceed the capture threshold, then the permeability of the myocardial cells will not be altered and thus no depolarization will result. If, on the other hand, the energy of the pacing stimulus exceeds the capture threshold, then the permeability of the myocardial cells will be altered such that depolarization will result. Changes in the capture threshold may be detected by monitoring the efficacy of stimulating pulses at a given energy level.
The ability to detect capture in a pacemaker is extremely desirable in that delivering stimulation pulses having energy far in excess of the patient's capture threshold is wasteful of the pacemaker's limited power supply. In order to minimize current drain on the power supply, it is desirable to automatically adjust the pacemaker such that the amount of stimulation energy delivered to the myocardium is maintained at the lowest level that will reliably capture the heart. To accomplish this, a process known as "capture verification" must be performed wherein the pacemaker monitors to determine whether an evoked depolarization or R-wave occurs in the heart following the delivery of each pacing stimulus pulse.
The conventional pacemaker typically includes a pacing output circuit designed to selectively generate and deliver stimulus pulses through a lead to one or more electrodes positioned in the heart of a patient. The pacing output circuit includes a power supply, switches, a pacing charge storage capacitor, and a coupling capacitor, all of which cooperatively operate under the direction of a microprocessor-based controller to perform a charging cycle, a pacing cycle, and a recharging cycle. The capacitance of the pacing charge storage capacitor typically ranges between 10-30 microfarads so as to develop a sufficient pacing charge for stimulating the heart ranges. The capacitance of the coupling capacitor typically ranges between 15 to 40 microfarads with 33 microfarads being typical. A capacitor having a capacitance in this range was believed necessary to deliver sufficient energy to the heart.
The charging cycle involves manipulation of the switches such that the pacing charge storage capacitor is charged up to a predetermined voltage level. The pacing cycle involves manipulating the switches such that the voltage within the pacing charge storage capacitor may be discharged through the coupling capacitor to the electrodes of the pacemaker. The recharging cycle involves further manipulation of the switches for a predetermined period of time following the pacing pulse to allow the coupling capacitor to be discharged.
While the conventional pacing circuit is generally effective in delivering stimulus pulses to the heart, it has been found that the detection of evoked depolarization or "capture verification" is rendered very difficult due to polarization voltages or "afterpotentials" which develop at the heart tissue/electrode interface following the application of the stimulation pulses. The inventors in the present application have discovered that these polarization voltages are due, in large part, to the relatively large capacitance of the conventional coupling capacitor. In the past, the large capacitance of coupling capacitor was believed necessary in order to sufficiently block any DC components from the heart and to minimize pace pulse voltage droop. However, the large capacitance of the coupling capacitor causes a charge dissipation or "afterpotential" which is relatively large (100 mV or greater) and which decays exponentially over a relatively long period of time (100 milliseconds). This is particularly troublesome due to the fact that the evoked potential or R-wave of the heart tissue is small in amplitude (5-20 mV) relative to the polarization voltage or "afterpotential" (100 mV). Moreover, the long decay period of the polarization voltage or "afterpotential" effectively masks the evoked potential or R-wave, which typically begins within approximately (10-20) milliseconds after the stimulation pulse. It will be appreciated that this creates difficulty in detecting the evoked response or R-wave of the heart following the delivery of stimulus pulses. In that evoked response is indicative of capture, the undesirable masking of the evoked response by "afterpotentials" thus hampers the ability of the pacemaker to conduct automatic capture verification. Hence, there is a need for a pacing output circuit that shortens the pacing afterpotentials with minimal increase of the leading edge voltage pacing threshold.
The prior art is replete with patents which address the problem of polarization voltage or "afterpotentials" hindering capture verification in cardiac pacing systems. U.S. Pat. No. 4,373,531 to Wittkampf et al. teaches the use of pre and post stimulation recharge pulses to neutralize the polarization on the pacing lead. U.S. Pat. No. 4,674,508 to DeCote, Jr. teaches the use of paired pacing pulses wherein the waveforms sensed through the pacing lead following the generation of each of the pair of pulses are electronically subtracted to yield a difference signal indicative of the evoked cardiac response. The approaches of the '531 patent and the '508 patent are unnecessarily wasteful of battery power and unduly complex due to the need to deliver opposite-polarity charges and pairs of closely spaced pacing pulses, respectively, to the electrode.
U.S. Pat. No. 4,399,818 to Money teaches the use of a direct-coupled output stage wherein polarization voltages at the heart tissue/electrode interface are dissipated, by shorting the electrodes together. U.S. Pat. No. 4,498,478 to Bourgeois teaches the use of a resistor across the output terminals (electrodes) such that a current path is provided for discharging and recharging the effective capacitance at the electrode/tissue interface. U.S. Pat. 4,537,201 to Delle-Vedove et al. teaches a linearization of the exponentially decaying sensed signal by applying the sensed signal through an anti-logarithmic amplifier in order to detect a remaining nonlinear component caused by the evoked potential. The approach of the '201 patent is disadvantageous in that it requires unnecessarily complex circuitry that is difficult to implement to produce the anti-logarithmic amplifier. U.S. Pat. No. 4,821,724 to Whigham et al. teaches the use of a triphasic stimulus having two positive pulses and one negative pulse for balancing the charge at the electrode/tissue interface.
U.S. Pat. No. 4,686,988 to Sholder teaches the use of a separate sensing electrode connected to a detector for detecting P-waves in the presence of atrial stimulation pulses, wherein the P-wave detector has an input bandpass characteristic selected to pass frequencies that are associated with P-waves. U.S. Pat. No. 4,858,610 to Callaghan et al. teaches the use of charge dumping following delivery of the stimulation pulse to decrease lead polarization and also the use of separate pacing and sensing electrodes to eliminate the polarization problem on the sensing electrode. The techniques of the '610 patent and '988 patent, which involve using a separate electrode located at some distance from the stimulating electrode for the purpose of isolating the polarization voltages or "afterpotential," are not completely desirable in that they require the additional cost and complexity of the additional sensing electrode.
U.S. Pat. No. 5,324,310 to Greeninger et al. teaches the use of the "ring-to-ring" sensing with corresponding atrial and ventricular EGM amplifiers whose outputs are multiplied and compared to a predetermined threshold to determine capture. U.S. Pat. No. 5,486,201 to Canfield discloses an active discharge circuit having a switching device which sequentially and repeatedly couples a charge transfer capacitor to the coupling capacitor to transfer charge therebetween and thereby actively discharge the coupling capacitor. None of these devices reduce or shorten the pacing afterpotentials through the use of a simplified pacing output. The present invention addresses these and other needs that will become apparent to those skilled in the art.